There have recently been many clinical reports that active oxygen and free radicals do damage to the membrane tissue of a living body, and this damage participates in the cause of various diseases such as cardiopathy, inflammation, cancer and ischemic disorder.
Active oxygen in vivo includes a superoxide radical (O.sub.2.sup.-), hydrogen peroxide (H.sub.2 O.sub.2), a hydroxyl radical (.OH) and singlet oxygen (.sup.1 O.sub.2) in an excited state.
As mechanisms for scavenging the active oxygen in vivo, it is considered that the superoxide radical (O.sub.2.sup.-) and hydrogen peroxide (H.sub.2 O.sub.2), which have a relatively long life, are scavenged by enzymes, and the other active oxygen, which has a short life, is scavenged by low-molecular weight compounds such as ascorbic acid. For example, a superoxide radical (O.sub.2.sup.-) formed in an erythrocyte is almost all scavenged by superoxide dismutase (SOD), hydrogen peroxide (H.sub.2 O.sub.2) is scavenged by catalase and peroxidase, and singlet oxygen (.sup.1 O.sub.2) is scavenged by .beta.-carotene and tocopherol.
However, there has not been yet developed any low-molecular weight compound capable of directly scavenging a hydroxyl radical which is considered to have high reactivity and also be the greatest in organism-damaging action among the active oxygen. Further, it is considered that since the hydroxyl radical reacts to cell components at a rate almost near a diffusion controlled rate, its life is short, so that the organism itself cannot have a special mechanism capable of scavenging this radical.
The formation of the hydroxyl radical in vivo is considered to be caused by the reaction of hydrogen peroxide (H.sub.2 O.sub.2) with the superoxide radical (O.sub.2.sup.-) as represented by the following reaction formula: ##STR1## Namely, when an respiratory substrate is oxidized in a mitochondrion of a cytoplasm, the electron of the substrate is transferred to an electron transport system in the exact order, and finally transferred to an oxygen molecule (O.sub.2) by cytochrome oxidase to form water (H.sub.2 O). The O.sub.2 molecule in the mitochondrion is reduced by 4 electrons to cleave the O.sub.2 molecule into two H.sub.2 O molecules. The mechanism of this catalytic action is not yet completely elucidated. However, a reaction easy to occur is the formation of H.sub.2 O.sub.2 by reduction of O.sub.2 with 2 electrons. H.sub.2 O.sub.2 is reacted with O.sub.2.sup.- to form .OH, a sort of active oxygen high in reactivity. On the other hand, various investigations as to SOD or SOD-like active substances, which catalyze the disproportionation of a superoxide radical (O.sub.2.sup.-), have been carried out. However, such catalytic substances involve a problem from the viewpoint of stability, and do not directly scavenge the hydroxyl radical. As scavengers capable of directly scavenging the hydroxyl radical, there have been known a hydroxyl radical scavenger comprising nicorandil as an active ingredient as described in Japanese Patent Application Laid-Open No. 101621/1991, an active oxygen scavenger comprising sesamin or the like as an active ingredient as described in Japanese Patent Application Laid-Open No. 227977/1994, and the like. However, no one has yet succeeded in making their products. As a model for a myocardial damage by a hydroxyl radical, there is a model of cardiac functional and myocardial metabolic disorder induced by the perfusion of H.sub.2 O.sub.2 using the heart enucleated from a rat (Am. J. Physiol., Vol. 265, No. 5, H1478-1485 (1993)). In this model, it has been reported that lidocaine having antiarrhythmic action and membrane-stabilizing action exhibits an improving effect in a concentration of 50-200 .mu.M.
Accordingly, it is an object of the present invention to provide a substance having a directly scavenging action on a hydroxyl radical and a medicine composition capable of treating various diseases by such an action.